Abstract

Introduction

Many studies suggest that elevated triglyceride levels are associated with increased long-term risk of stroke, including transient ischemic attacks. In addition, elevated triglyceride levels independently contribute to plasma viscosity and decreased blood flow. However, no consensus has been reached regarding the significance of hypertriglyceridemia as an independent risk factor for ischemic stroke.

Conclusions

The findings in our patient’s case are likely explained by triglyceride-mediated hyperviscosity causing a transient ischemic attack. In the present report we suggest that when several tests do not reveal the cause of stroke-like symptoms, measurement of plasma viscosity may be informative.

Electronic supplementary material

Introduction

Elevated triglyceride levels are associated with increased long-term risk of ischemic stroke[1]. Short-term complications include pancreatitis, which is an emergent problem, and other complications that have been reported in familial hypertriglyceridemia, including recent memory loss, abdominal pain, dyspnea, eruptive xanthoma, flushing after alcohol consumption, and lipemia retinalis[2]. However, no consensus has been reached regarding the significance of hypertriglyceridemia as an independent risk factor for ischemic stroke[3]. Here, we report the case of a patient with sudden coma likely caused by triglyceride-mediated hyperviscosity.

Case presentation

A comatose 56-year-old Japanese man with no significant familial medical history was admitted to the emergency room. He delivered newspapers and usually consumed alcohol two hours before delivery. According to colleagues, during his usual morning routine, he suddenly fell on his back. On admission, his temperature was 36.0°C, pulse rate 77 beats/min, blood pressure 153/94mmHg and Glasgow Coma Scale score was E2V2M1. On examination, splenohepatomegaly was detected, but heart murmur, chest rales, tongue biting, incontinence, diaphoresis, seizure, and xanthoma were not evident. He maintained a balanced diet and was not obese (height 164cm, weight 58.8kg and body mass index 21.9kg/m2).

Hypertriglyceridemia can occur because of obesity, poorly controlled diabetes mellitus, alcohol misuse, and familial disease. In our patient’s case, he had no family history, and therefore, the causes of hypertriglyceridemia were likely to be poor control of diabetes mellitus and alcohol misuse. Many case reports and series have described apheresis for hypertriglyceridemia. However, we did not pursue this treatment because our patient responded to fluid therapy and did not exhibit pancreatitis.

The effects of alcohol and alcohol withdrawal cannot be ruled out in our patient. However, people with chronic alcoholism may demonstrate little clinical evidence of intoxication even with blood alcohol levels >22.2mmol/L[8]. In addition, alcohol withdrawal cannot explain the symptoms, because withdrawal symptoms typically begin four to 12 hours after alcohol cessation. Our patient’s symptoms appeared two hours after consumption, and his vital signs and physical characteristics did not indicate alcohol withdrawal. With regard to hyperglycemia, symptoms of hyperosmolar hyperglycemic state develop insidiously with polyuria, polydipsia, and weight loss, often persisting for several days before hospital admission, and diabetic ketoacidosis usually evolves more rapidly, over a 24-hour period. In our patient’s case, his symptoms developed too quickly and his β-hydroxybutyric acid level was normal. Therefore, the probability of hyperglycemia being the direct cause of his coma is low.

Conclusions

We report the case of a patient who entered coma, likely caused by triglyceride-mediated hyperviscosity causing a transient ischemic attack. We suggest that when several tests do not reveal the cause of stroke-like symptoms, measurement of plasma viscosity may be informative.

Consent

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Notes

Acknowledgements

We would like to acknowledge Makiko Hirahata and Shigemi Kobayashi for their assistance.

Copyright information

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.